G CSF Mouse

The mouse G-CSF was first recognized and purified in 1983 at the Walter and Eliza Hall Institute in Australia . This discovery paved the way for further research into its human counterpart, which was cloned by groups from Japan, Germany, and the United States in 1986 . The recombinant form of G-CSF has since been developed and used in numerous therapeutic contexts.

G-CSF functions by binding to its specific receptor on the surface of hematopoietic cells. This binding activates several intracellular signaling pathways that lead to the proliferation, differentiation, and survival of neutrophil precursors . Additionally, G-CSF has been shown to have anti-apoptotic effects, immunomodulatory actions, and the ability to stimulate neurogenesis and angiogenesis .

G-CSF is widely used in clinical practice, particularly in the treatment of neutropenia, a condition characterized by an abnormally low count of neutrophils. Neutropenia often occurs as a side effect of chemotherapy, and G-CSF helps to increase the neutrophil count, thereby reducing the risk of infection . It is also used to mobilize hematopoietic stem cells for transplantation .

In research, mouse recombinant G-CSF is used to study various aspects of hematopoiesis and immune responses. It has been employed in pre-clinical studies to investigate its potential therapeutic effects in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) . These studies have shown that G-CSF can induce neuronal regeneration, inhibit neuronal apoptosis, and regulate inflammatory cytokines .